Identification of the genes associated with virulence in Aspergillus species: Aspergillus species cause substantial morbidity and mortality in humans principally among those compromised by chronic granulomatous disease (CGD) or prolonged neutropenia. Although it is known that aspergillosis is caused by inhaled conidia, little is known about the precise events and interactions with the host that lead to successful survival and propagation of the fungus. Aspergillus conidia (spores) are known to be covered by a layer of hydrophobic proteinaceous fascicles called rodlets. The rodlet layer is believed to be responsible for the hydrophobic nature and the dispersibility of the spores. It has been shown that resting conidia of A. fumigatus with intact rodlet layers are killed much less effectively by human neutrophils than the swollen, rodletless hydrophobic conidia. It has also been shown that hydrophilic conidia are more susceptable to neutrophil oxidative products and rabbit neutrophil cationic peptides. In addition, macrophages are also less able to kill hydrophobic spores than hydrophilic spores. In the previous year we have cloned the HYP1 gene responsible for the formation of rodlet layer in A. fumigatus and showed that it is expressed in A. nidulans another Aspergillus pathogen primarily affecting CGD patients. The second gene responsible for the hydrophobicity of A. nidulans conidia was cloned by Stringer et. al., recently. This year we studied the effect of hydrophobins on fibrinigen binding and alternative complement pathway- mediated opsonization using hydrophobin gene disrupted mutants of A. nidulans. The results suggested optimal fibrinogen binding requires an intact hydrophobin layer of conidia and that competition takes place between fibrinogen and complement-uptake on conidial surfaces. These results indicate that hydrophobins on the conidial surface play an important role in the opsonophagocytosis of Aspergillus conidia.